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Medicine > Oncology > Flashcards

Oncology Flashcards

1
Q

Child growing up in Africa presenting with unilateral jaw swelling- what is the likely diagnosis?

A

Burkitt’s lymphoma (endemic type)

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2
Q

Types of Burkitt’s lymphoma

A

Endemic (african): jawline/head/neck, 95% chance of EBV

Sporadic: abdomen, 10-15% chance of EBV

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3
Q

Specific Mutation commonly seen in childhood lymphoma

A

Burkitt’s lymphoma- t(8;14) (q24;q32) reciprocal translation -> C-MYC (Chr8) to Ig heavy chain locus (Chr14). Seen in 80% of Burkitt’s lymphoma

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4
Q

What is the philadelphia chromosome? What is it associated with?

A

Philadelphia chromosome = t(9;22)
translocation creating BCR-ABL1 causing constitutive activation of Tyrosine kinase to allow unregulated cell division.
Associated with Chronic Myeloid Leukaemia (95% of people with CML have BCR-ABL1) but also seen in Acute Lymphocytic Leukaemia (rarely in AML)

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5
Q

Oncogene examples

A

RAS, WNT, MYC, ERK, TRK, RET, c-SIS, Raf-kinase, CDKs,
Rtks: EGFR/HER-1, PDGFR, VEGFR, HER2/neu
PI3KCA
Akt1

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6
Q

Tumour suppressor gene examples

A

Rb, p53, INK4/PTEN, APC, CD95, pVHL

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7
Q

Drugs targeting hallmarks of cancer?

A

PARP inhibitors: olaparib (for genome instability/mutation)
EGFR inhibitors: cetuximab, gefetinib for sustained proliferative signalling)
VEGF signal inhibitors: bevacizumab (anti-angiogenesis)
Anti-CTLA4 mAb: ipilimumab (immune activating)

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8
Q

What is herceptin?

A

Trastuzumab = anti HER2 humanised mouse monoclonal antibody

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9
Q

New drug target in melanoma?

A

B-RAF kinase inhibitors: sorafenib and veramurafenib

B-RAF = Proto-oncogene in MAPK pathway (mutated in 50-60% of melanomas)

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10
Q

Example of targeted cancer immunotherapy?

A

Programmed cell death receptor (PD-1) and PD-L1 (ligand) overexpressed in many tumours -> decreased cytokine production.
Pembrolizumab and Nivolumab inhibit PD-1 receptor (but severe toxicity)
Ipilimumab anti- CLTA4 antibody. Turns off inhibition of CTLs.

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11
Q

What is taxol?

A

Inhibitor of mitotic spindle activity, target Tubulin.

Uses: solid cancers (ovary, breast, lung, bladder, prostate, melanoma, oesophageal) + Kaposi’s Sarcoma.

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12
Q

Common mutation seen in melanoma?

A

B-raf constitutively active in 40-60%

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13
Q

New drug for melanoma?

A

Vemurafenib. B-RAF enzyme inhibitor (B-RAF-MEK step)

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14
Q

Nivolumab- how does it work? Uses?

A

Monoclonal antibody inhibiting PD-1 receptor (programmed cell death). Metastatic melanoma, squamous cell lung cancer, renal cell carcinoma.

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15
Q

What does ipilimumab do?

A

Monoclonal antibody to CTLA4 receptor (normally inhibits cytotoxic T cells)

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16
Q

What is pembrolizumab?

A

Humanised mouse monoclonal antibody to inhibit PD-1 receptor (programmed cell death) inducing T cell attack.

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17
Q

Common mutation in NSCLC?

A

Activating EGFR mutation 10-30% (high in non-smokers, adenocarcinoma histology, higher in Japan)
ALK fusion oncogene. (Receptor tyrosine kinase)

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18
Q

What is erlotinib?

A

Oral EGFR tyrosine kinase inhibitors. Used for specific NSCLCs.

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19
Q

What is gefitinib?

A

Oral EGFR tyrosine kinase inhibitor used for certain types of NSCLC.

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20
Q

Pathways activated by EGFR?

A

PI3K -> AKT -> mTOR -> survival
JAK -> STAT ->survival
RAS -> RAF -> MEK -> ERK -> Proliferation

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21
Q

What is glivec?

A

Imatinib: small molecular inhibitor of BCR-ABL (constitutively active tyrosine kinase) in CML and c-KIT in GISTs.

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22
Q

What is a complete response to treatment?

A

RECIST for solid tumours

Disappearance of all target lesions.

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23
Q

What is a partial response to treatment?

A

30% decrease in sum of the longest diameter of target lesions

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24
Q

What is stable disease v progressive disease in solid tumours?

A

Progressive disease: 20% increase in sum of the longest diameter of target lesions
Stable disease: small changes that do not meet partial response (30% decrease) or progressive disease criteria.

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25
Q

When do we expect Resistance to therapy?

A

After 10-12months of response to targeted therapy. (Mostly due to ‘steric hindrance’)

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26
Q

How does radiotherapy work?

A

High energy X-rays interact and produce high energy electrons -> damage DNA directly (ss/ds breaks) and indirectly (cause water -> H. OH. Radicals -> ss/ds breaks)

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27
Q

Side effects fo radiotherapy?

A

Acute toxicity: after 2w, dermatitis, stomatitis and enteritis. Nausea and fatigue, hair loss (2-3w).
Late toxicity: vascular injury to normal tissues, small vessel obliterative endarteritis and fibrosis.
Growth: premature fusion and loss of stature in children.
Risk of second malignancy: 3% per decade for kids, 1% per decade for adults

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28
Q

How to get maximum radiotherapy dose to tumour?

A

Conformal: shape the dose
Fractionation of therapy: daily treatments
Enhance by using chemo therapy (chemo-radiotherapy) radiosensitiser.

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29
Q

Example of nitrogen mustard? MOA?

A

Cyclophosphamide, melphalan, chlorambucil, bendamustine

MOA: DNA alkylators

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30
Q

Alkylating agents for chemotherapy?

A

Nitrosoureas: nimustine, carmustine, lomustine
Triazene: dacarbazine, procarbazine, streptozotocin - alter bases
Nitrogen mustards: chlorambucil, cyclophosphamide, melphalan, bendamustine
Aziridines: Mitomycin C, thiotepa
Modify purines, guanine/adenine alkylation and chemical crosslinking.

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31
Q

Antifolate and purine analogues for cancer therapy?

A

Antifolates: methotrexate (DHFR)
Purine analogues: 5-fluoro-uracil.
PrPP/GARFT pathway: 6-mercaptopurine

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32
Q

Platinum agents in cancer therapy? Which? MOA?

A

Cisplatin, carboplatin

MOA: intrastrand DNA cross-link, interstrand DNA cross-link, DNA histone crosslinks, induction of apoptosis.

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33
Q

Anthracyclines in cancer therapy?

A

Doxorubicin, (red fungus from adriatic)

Intercalates into DNA and inhibits Topoisomerase I and induces free radicals. Cardiotoxic

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34
Q

What are taxanes?

A

Taxol/paclitaxol. Microtubule formation inhibitor = mitotic arrest.
Not water soluble. (Frequent systemic allergic response)
Used for solid tumours

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35
Q

What are Camptothecins?

A

Topoisomerase I inhibitors. (Prevents DNA uncoiling before replication). Irinotecan/topotecan.

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36
Q

What is gemcitebine?

A

Synthetic nucleoside analogue (instead of C- blocks DNA synthesis)
Uses: bladder/urothelial. Pancreatic cancer.
Causes early neutropaenia

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37
Q

What is the difference between cytocidal and cytostatic agents?

A

Cytocidal: direct reduction in number of clonogens, kills cells. Mainly during replication
Cytostatic: prevents tumour growth, inhibiting growth signal or disrupt blood supply. Cell kill secondary.

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38
Q

What type of agents are cytocidal, cytostatic?

A

Cytocidal: most chemotherapy
Cytostatic: many biological therapies

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39
Q

What affects sensitivity of tumours to cytotoxic agents? Which tumours?

A

Rate of cell division.
High: lymphoma, leukaemia, SCLC, testis
Mid: Breast, colorectal, NSCLC
Low: HNSCC, prostate, stomach, pancreas, glioma

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40
Q

What is an important consideration when treating Burkitt’s lymphoma?

A

Burkitt’s lymphoma is very sensitive to chemo- beware of tumour lysis syndrome (hyperuricaemia, renal failure)

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41
Q

How does the number of cells killed by cytoxic agents change with doses?

A

Constant FRACTIONof cells killed by a certain dose of drug. Need repeated doses for tumour control.

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42
Q

Difference in adjuvant v curative primary chemotherapy?

A

Curative chemo: enough doses to reduce tumour cell number to zero through cumulative cell kill.
Adjuvant: less doses need to bring tumour clonogen number to zero.

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43
Q

How do we generally dose chemotherapy?

A

Body surface area (decent surrogate for drug clearance)
Biologics may be dosed by body weight.
Carboplatin dosed by GFR

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44
Q

What is MTD? What is LC50?

A

MTD: maximum tolerated dose (of chemo)
LC50: lethal concentration determined in animal models.

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45
Q

Why 3 weekly cycles of chemo?

A

3 weeks for bone marrow to recover.

46
Q

What is dose intensity? Dose density?

A

Intensity: increasing dose a little
Density: decrease interval between doses.

47
Q

Complication of procarbazine?

A

Delayed bone marrow suppression (given 6weekly cycle)

48
Q

How to ablate bone marrow?

A

High dose chemo (above MTD) then rescue with stem cell transplant

49
Q

What is primary restistance to chemotherapy?

A

No response from the start

50
Q

What is acquired resistance in chemotherapy? What do you do about it?

A

Adaption/mutation of tumour clonogens.

Combination chemo/sequenced chemo to overcome resistance.

51
Q

Mechanisms of acquired tumour resistance?

A
  • enhanced drug efflux (p-glycoproteins transporters)
  • Multidrug resistance protein
  • Compartmentalisation (reduced uptake of agent to nucleus)
  • Upregulate target enzyme/pathway
  • rapid repair of DNA lesions
  • Abrogation of apoptosis pathway
52
Q

Mechanism of nausea in chemo?

A

Area postrema near 4th ventricle. (No tight junctions in vessels: ‘samples’ circulating blood)

53
Q

Management of nausea/vomiting in chemo?

A

Ondansetron: 5HT3 antagonists

If needed can use Aprepitant (NK1 receptor antagonist)

54
Q

Highly emetogenic regimens?

A

Cisplatin, dacarbazine, streptozocin, ABVD, AC, BEP. = use 5HT3 antagonists

55
Q

Acute toxic effects of chemo?

A

Nausea and vomiting
Skin/mucosa: mucositis, alopecia, extravasation
Bone marrow: anaemia, neutropaenia, thrombocytopaenia
GI: Diarrhoea, constipation, typhlitis
Neuro: encephalopathy
Systemic allergic response
Tumour lysis syndrome

56
Q

What is typhlitis?

A

Neutropaenic enteritis

57
Q

Important effect of ifosfamide?

A

Encephalopathy

58
Q

Important early effect of taxanes?

A

Systemic allergic response

59
Q

Signs of tumour lysis syndrome?

A

Hyperkalaemia
Hyperuricaemia
Metabolic acidosis
Renal failure

60
Q

How to avoid tumour lysis syndrome?

A

Prehydration, give chemo slowly
Urinary alkalinisation (allows increased uric acid secretion)
Allopurinol before chemo (inhibits uric acid production)

61
Q

Late toxic effects of chemo?

A

Cardiac, renal, hepatic, lung fibrosis, nerve toxicity and deafness, fertility impairing, carcinogenicity and teratogenicity.

62
Q

Important late effect of bleomycin?

A

Lung fibrosis

63
Q

Chemo agents causing nerve toxicity and deafness?

A

Vincristine, oxaliplatin, cisplatin

64
Q

Important late effect of anthracyclines?

A

LVEF

65
Q

Important late effect of 5-FU?

A

Coronary arteries affected

66
Q

Chemo agents toxic to kidney late?

A

Cisplatin, carboplatin,
Carmustine
Methotrexate (high dose)

67
Q

Types of biological therapies?

A

Monoclonal antibody therapies (-ab)
Small molecular inhibitors of tyrosine kinases (-ib)
Non-specific immune activation (interferon, interleukin)
Specific vaccines

68
Q

What is a targeted biological therapy?

A

Targeted to pathway highly upregulated or specific to cancer cells.

69
Q

Mechanism of monoclonal agents action?

A

PN humanised monoclonal -> immune activation by CTLA-4 binding and cytotoxic T cell activation.

70
Q

What is avastin?

A

Bevacizumab: monoclonal to VEGF-A. Prevents VEGFR-2 binding. Use: colon, lung, breast, kidney, GBM, AMD.

71
Q

Problem with avastin?

A

Pseudoresponse: initial dramatic response, not maintained. Initial separation of survival curves lost at 12m.
Other issues: impaired wound healing, HTN, proteinuria, renal injury

72
Q

What is herceptin?

A

Trastuzumab: Monoclonal antibody to HER-2/neu receptor (prevents EGF binding)
Use: HER2+ metastatic or high risk breast cancer

73
Q

Important problem with herceptin?

A

Rare myocardial toxicity. (Espcially if prior anthracyclines treatment)

74
Q

What is gefitinib?

A

Iressa/gefitinib: inhibits Tyrosine kinase of EGFR.

Useful for EGFR + mutation NSCLC

75
Q

What is Glivec?

A

Glivec/Imatinib: tyrosine kinase inhibitor for BCR-ABL fusion protein (constitutively active). Philadelphia chromosome + CML.
Also Used for GISTs: targets c-KIT

76
Q

How to see response to glivec?

A

PET imaging. Tumours may be same size on CT.

77
Q

Is resistance a problem in biological therapies?

A

YES: resistance to Tyrosine Kinase inhibitors after approx 8-12months. (By steric hindrance)

78
Q

Pt currently being treated for cancer presents to ED: what is the most important question you want to know?

A

Are they on curative or palliative treatment

79
Q

Definition of neutropaenic sepsis?

A
  1. ANC (absolute neutrophil count) <0.5 (or less than 1.0 and expected to go <0.5) AND
  2. A: Temp >38C on 2 occasions or >38.5 once OR
  3. B: Hypotension, desaturation, organ failure
80
Q

Pt being treated for metastatic colorectal cancer presents to ED feeling rubbish. Day before new cycle of chemo. Differentials?

A

GI Gram negative neutropaenic sepsis-> tazocin
Urosepsis
Pneumonia

81
Q

Likely causative organism in pt treated with PICC for cancer? Which antibiotic to use?

A

Staphylococcal sepsis -> use vancomycin

82
Q

Organisms seen in haematological cancer treated patient

A

Fungal infections (including pneumocystis pneumonia)

83
Q

Cancer pt presenting with appendix like symptoms - differentials?

A

Perforation
Neutropaenic enteritis
Appendicitis

84
Q

Management of ?neutropaenic sepsis?

A 
Peripheral and central blood cultures
IV antibiotics (piperacillin/tazobactam)
\+ gentamycin if hypotensive
\+ vancomycin if PICC/portacath
4hrly Obs + MEWS 
\+ GCSF if pt is shocked
Regular review
DON'T do a PR = risk of bacteraemia
85
Q

Signs of malignant hypercalcaemia?

A

Bones (bone pain, even if no mets), stones (renal stones, hypercalinuria), groans (abdo pain), psych moans (depression), malaise

86
Q

Best Clinical indication of spinal cord compression?

A

Short history of radicular (band-like) pain with a sensory level.

87
Q

Signs/symptoms of spinal cord compression?

A 
Pain +sensory level.
Bone tenderness
Distal weakness
Hyper-reflexia
Bladder and bowel disturbance
88
Q

Management of spinal cord compression?

A

Analgesia, bed rest
Start dexamethasone to reduce cord inflammation and oedema
Urgent MRI spine with contrast (or CT myelogram if pacemaker)
(Catheter)
Refer to MSCC
Surgery or radiotherapy.

89
Q

Why choose surgery or radiotherapy in malignant spinal cord compression?

A

Surgery: best for single level disease (especially if vertebral collapse -> restore vertebral geometry)
Radiotherapy: for extensive multi-level disease, poor performance status/high disease burden or soft tissue masses

90
Q

Causes of malignant hypercalcaemia?

A

Diffuse bone disease

Paraneoplastic syndrome from ectopic PTHrP (lung cancer/NET)

91
Q

Treatment of malignant hypercalcaemia?

A 
Fluid rehydration (4l or more -> pt euvolaemic)
Bisphosphonate therapy (inhibits osteoclasts activity) may be also used to prevent hypercalcaemia and fractures
Treat tumour (good for refractory hypercalcaemia)
92
Q

Tumours at risk of tumour lysis syndrome:

A

Burkitt’s Lymphoma

Germ cell tumours

93
Q

Treatment of tumour lysis syndrome?

A

Rasburicase: recombinant uric oxidase (urate -> allantoin =10x more soluble and excretable) BUT expensive

94
Q

Causes of hyponatraemia in cancer patients?

A

Corticosteroid induced hyponatraemia (given in advanced disease)
Pt with losses: 3rd space-oedema, D+V
Disease in lung, liver, brain
SIADH from ectopic ADH production

95
Q

How to differentiate the causes of hyponatraemia in malignancy?

A

Hypovolaemic hyponatraemia: steroids, D+V, oedema, ext disease.
Euvolaemic hyponatraemia: SIADH
Technically true but difficult to use clinically (e.g. Dehydrated patient, non specific symptoms)
-> PAIRED URINE PLASMA OSMOLALITY

96
Q

Expected result in SIADH of paired urine and plasma osmolality?

A

Inappropriately concentrated urine for hyponatraemia

97
Q

How to manage ?SIADH?

A

Treat underlying malignancy

Liaise with endocrinology re fluid restriction and democlocycline (tubular poison)

98
Q

Important neuro sign of hydrocephalus?

A

False localising CNVI palsy

99
Q

Signs/symptoms of raised ICP?

A 
Headache (on waking in morning) 
Nausea
Seizures
Focal neuro deficit (false localising CNVI palsy)
Behavioural change
Fluctuating level of consciousness
Papilloedema
100
Q

Radiological signs of acutely raised ICP?

A

Dilated ventricles, sulci NOT effaced

Periventricular fluid transudation (bright on T2) ‘capping sign’

101
Q

How to diagnose ?hydrocephalus?

A

Urgent CT

102
Q

Management of hydrocephalus?

A

Ommaya reservoir: fluid drainage at bedside, allows intrathecal chemo
Ventriculo-peritoneal shunt: long term if chronic hydrocephalus. Programmed valve. (No longer ventriculoatrial shunts -sepsis)
Endoscopic third ventriculostomy: for tumour blocking ventricular outflow, CSF to basal cisterns,

103
Q

Likely cause of SVCO today?

A

Bulky mediastinal lymph nodes in SCLC. (Previously syphilitic aortitis)

104
Q

Pt with lung cancer presents with dyspnoea, headache, dizziness. Differentials?

A 
SVCO
Progression
Hydrocephalus/raised ICP
Pneumonia
Cardiac disease?
105
Q

Signs of SVCO?

A

High venous pressure
Headache and dizziness
Facial swelling and redness
(Dilated veins of chest wall if longer time span)

106
Q

Management of SVCO?

A

Sit up
Oxygen (high flow)
High dose steroids
- clinical diagnosis (CXR/CT for confirmation)
Discuss with interventional radiologists ?stent OR start definitive treatment if a mural thrombus.

107
Q

What circumstances would allow you to not discuss DNACPR?

A

‘Serious physical or psychological harm’

108
Q

Cancers that metastasise to bone?

A 
Breast
Kidney
Thyroid
Bronchus
Prostate
109
Q

Cytokeratin markers for breast cancer?

A

CK7+, Oestrogen-R +, Progesterone-R +

110
Q

Cytokeratin markers for breast cancer?

A

CK7+, Oestrogen-R +, Progesterone-R +

Medicine (16 decks)

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